AB0612 Chronic pancreatitis due to systemic autoimmune and bacterial septic vasculitis in rheumatoid arthritis – A hypothetic pathway of chronic pancreatitis in post-Covid 19 condition
Authors: Á. Apáthy, M. Bély
Journal: Annals of the Rheumatic Diseases (2022)

Background The etiology of pancreatitis is heterogeneous; it may be due to chronic excessive alcohol use, gallstones, medications, infections, autoimmune diseases, metabolic disorders, trauma, congenital malformations etc. Objectives The aim of this study has been to describe a hypothetic pathway of chronic pancreatitis in post-Covid 19 condition, based on the role of autoimmune and bacterial septic vasculitis in the pathogenesis of chronic pancreatitis ( ChrP ) in rheumatoid arthritis ( RA ). Methods At the National Institute of Rheumatology 9475 patients died between 1969 and 1992; among them 161 with RA and all of them were autopsied. RA was confirmed clinically according to the criteria of the ACR . Tissue samples of pancreas were available for histologic evaluation in 111 patients. Pancreatitis and vasculitis were determined and characterized histologically [1,2]. The possible role of autoimmune vasculitis and bacterial septic vasculitis in the pathogenesis of ChrP was analyzed by Pearson’s chi-squared (χ 2 ) test. Results ChrP – characterized by diffuse and/or focal fibrosis and atrophy – was present in 10 ( 9.01 %) of 111 patients. Systemic vasculitis complicated RA in 28 (25.23%) of 111 patients. Twenty-five (89.3 %) of 28 systemic vasculitis proved to be of autoimmune origin. Autoimmune vasculitis involved the pancreatic blood vessels ( pAV ) in 8 (32.0 %) of these 25 patients. Non-specific (n=37), fibrinoid necrotic (n=14), and granulomatous type (n=5) of pAV were detected side by side in the same histologic section, involving pancreatic arteries of different sizes. The veins and venules were not involved. pAV was not associated with chronic pancreatitis. The relationship between pAV and ChrP was inverse with a negative colliquation coefficient (c=-1.0, χ 2 =0. 0801, p &lt;0.7772 – NS). Three (10.7 %) of 28 systemic vasculitis cases proved to be of septic (bacterial) origin. Pancreatic blood vessels ( pSV ) were involved in 2 (66.7 %) of these 3 patients. Granulomatous vasculitis was not seen with pSV , and the veins and venules were also spared. Non-specific (n=9), fibrinoid necrotic (n=2) vasculitis involving different size of pancreatic arteries were associated with chronic pancreatitis. The relationship between pAV and ChrP was significant (c=0.92308, χ 2 =6.3201, p &lt;0.012). Table 1. Prevalence of pAV / pSV Size of involved vessels Prevalence Ns pAV Prevalence Fn pAV Prevalence Gr pAV Total n/% of pAV Prevalence Ns pSV Prevalence Fn pSV Prevalence Gr pSV Total n/% of pSV Arteriole 18 10 3 31 – 55.36 3 0 0 3 – 27.27 small artery 16 4 2 22 – 39.28 3 2 0 5 – 45.46 medium size artery 3 0 0 3 – 5.36 3 0 0 3 – 27.27 Venule 0 0 0 0 – 0.0 0 0 0 0 – 0.0 small vein 0 0 0 0 – 0.0 0 0 0 0 – 0.0 medium size vein 0 0 0 0 – 0.0 0 0 0 0 – 0.0 Total 37 – 66.07% 14 – 25.0% 5 – 8.93% 56 – 100% 9 – 81.82% 2 – 18.18% 0 – 0.0 11 – 100% Conclusion Chronic pancreatitis is characterized clinically by abdominal pain and diarrhea, which are common in post-Covid 19 condition [2]. The strong and significant correlation between pSV and ChrP indicates that subclinical or manifest bacterial septic processes may play a role in the pathogenesis of ChrP . Hypothetically a similar pathway is plausible in post-Covid 19 chronic pancreatitis due to viral infection and vasculitis, analogous to bacterial septic vasculitis. Systemic vasculitis of autoimmune origin involving blood vessels of the pancreas may cause a special multifocal relapsing lipo-necrotic pancreatitis [1,2], and according to our results, do not influence the prevalence of ChrP . The autoimmune origin of pancreatic vasculitis may be excluded histologically by the presence of granulomatous vasculitis of the most frequently involved arterioles and small arteries. References [1]Bély M, Apáthy Á: Pathol Oncol Res, 2008;14(4):473-80. PMID: 18975138, DOI: 10.1007/s12253-008-9026-z [2] Bély M, Apáthy Á : Clinical pathology of rheumatoid arthritis. 1-440 pp. Akadémiai Kiadó, Budapest 2012 http://www.akkrt.hu [3] https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html Disclosure of Interests None declared